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      Insulin-Induced Arteriolar Dilation after Tyrosine Kinase and Nitric Oxide Synthase Inhibition in Hamster Cheek Pouch Microcirculation

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          We investigated the effects of tyrosine kinase (TK) and nitric oxide synthase (NOS) inhibition on insulin-induced dilation of arterioles. We determined the arteriolar diameter, red blood cell velocity (V<sub>RBC</sub>) and blood flow changes in hamster cheek pouch microcirculation as affected by insulin in presence of TK and NOS inhibitors, genistein, piceatannol and N<sup>G</sup>-monomethyl- L-arginine ( L-NMMA). Microvessels were visualized by a fluorescent microscopy technique. Arteriolar diameter and V<sub>RBC</sub> were measured after topical application of insulin and genistein or piceatannol or L-NMMA. Insulin (10 µU/ml) induced diameter and V<sub>RBC</sub> increase in A3 and A2 arterioles by 30 ± 5 and 123 ± 4%, 16 ± 4 and 102 ± 3%, as percent of baseline values, respectively. After genistein or piceatannol prior to insulin A3 and A2 arterioles dilated by 10 ± 4, 5 ± 2% and 9 ± 4, 2 ± 1%, respectively. After L-NMMA prior to insulin A2 and A3, arteriole diameters increased by 12 ± 3 and 7 ± 2%, respectively. V<sub>RBC</sub> increased significantly in all the cases. TK and NOS inhibitors applied together abolished insulin-induced dilation with a reduction in V<sub>RBC</sub> and blood flow. In conclusion, full insulin-induced dilation of hamster cheek pouch arterioles requires TK signaling pathways. Furthermore, activation of insulin receptors, as well as other TK receptors, appears to be required for vasomotor tone regulation.

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          Melatonin prevents ischemia reperfusion injury in hamster cheek pouch microcirculation.

          We used the hamster cheek pouch microcirculation to investigate the effects of melatonin (ME) on ischemia reperfusion (I-R) injury by in vivo microscopy. ME is a hormone produced by the pineal gland and is the most powerful and effective hydroxyl radical scavenger detected to date in vitro. The second aim was to determine the scavenger effect of ME in cheek pouch microcirculation when topically applying an oxygen-derived free radical generating system. Ischemia was induced by clamping the cheek pouch for 30 min followed by 30 min of reperfusion. We quantified the increase in permeability, the perfused capillary length and leukocyte adhesion by computerized methods. Microcirculation was also exposed to a hypoxanthine-xanthine oxidase (H-X) system. In control hamsters I-R was associated with increased permeability, increased number of leukocytes sticking to venules, and decreased perfused capillary length. Treatment with ME completely inhibited microvascular edema formation and reduced the number of leukocytes sticking to venules after reperfusion. Moreover, ME prevented the marked decrease in perfused capillary length, preserving microvascular perfusion. ME topically applied reduced significantly the permeability increase due to H-X exposure. The beneficial effect of ME may be related to its antioxidant properties. These protect the endothelial barrier integrity as well as preserve microvascular blood perfusion by dysfunctions after I-R.
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            Effects of L-NMMA and indomethacin on arteriolar vasomotion in skeletal muscle microcirculation of conscious and anesthetized hamsters.

            The purpose of this study was to determine the influence of NG-monomethyl-L-arginine (L-NMMA) and indomethacin (INDO), respectively inhibitors of nitric oxide synthase and cyclooxygenase, on spontaneous arteriolar activity (vasomotion) in the skeletal muscle of awake and anesthetized hamsters. Unanesthetized hamsters, implemented with the skin fold chamber window, displayed vasomotion, whose frequency and amplitude were quantified by power spectrum analysis. Intravenous administration of L-NMMA significantly increased vasomotion frequency and did not change the amplitude at the lower dose, but in order 3 arterioles amplitude decreased significantly. With higher doses L-NMMA caused constriction of order 1-2 vessels, frequency decreased and amplitude increased, and the arteriolar vasodilator response to acetylcholine decreased significantly. During anesthesia topically applied L-NMMA significantly decreased diameter and caused the appearance of vasomotion in order 1-2 arterioles. INDO did not affect vasomotion in unanesthetized hamsters and did not initiate vasomotion during anesthesia leading to the conclusion that prostaglandins do not regulate vasomotion. Vasomotion is not directly related to nitric oxide (NO) in conscious animals while NO blockage stimulates vasomotion in smaller arterioles of anesthetized hamsters without vasomotion; however, the simultaneous inhibition of cyclooxygenase and NO had no effect on arteriolar diameter during anesthesia. It is concluded that vasomotion is regulated by a mechanism that modulates smooth muscle cell activity through the endothelium.
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              Physical fitness and endothelial function (nitric oxide synthesis) are independent determinants of insulin-stimulated blood flow in normal subjects

               T Utriainen (1996)

                Author and article information

                J Vasc Res
                Journal of Vascular Research
                S. Karger AG
                August 1998
                07 August 1998
                : 35
                : 4
                : 250-256
                CNR Institute of Clinical Physiology, University of Pisa, Italy
                25591 J Vasc Res 1998;35:250–256
                © 1998 S. Karger AG, Basel

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                Page count
                Pages: 7
                Research Paper


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